Geology topics

Xinyuan Kang

Publications and source records attributed to Xinyuan Kang.

3 recordsLinked to original sources

USGS2025

Tetrabromobisphenol S (TBBPS) causes non-negligible and multigenerational reproductive toxicity in zebrafish

Tetrabromobisphenol S (TBBPS) is one of the most extensively used brominated flame retardants detected in the environment. Despite its widespread presence, the effects of persistent environmental exposure to TBBPS on the reproductive system remain unclear, raising significant health concerns. Here, using the zebrafish ( Danio rerio ) model, we identified significant intergenerational endocrine disruption and reproductive toxicity induced by TBBPS after a life-cycle (150 days) of parental exposure to environmentally relevant concentrations of TBBPS (0.01, 0.1, 1, 10, and 100 μg/L). TBBPS interfered with hormone levels and the expression of genes within the hypothalamic–pituitary–gonadal (HPG) axis in both F0 males and females, leading to reduced embryo quality. The parental transmission of TBBPS also impacted the endocrine and reproductive systems of the F1 fish, including the increase of gonadotropin-releasing hormone 3 neuron numbers, changes in hormone levels, and a decrease in embryo numbers. F2 fish also displayed endocrine disruption, even in the absence of detectable TBBPS residues, evidenced by altered fertilization rates and vitellogenin levels. Together, our findings show that exposure to environmentally relevant concentrations of TBBPS can induce reproductive toxicity that persists across generations, weakening the endocrine system and early growth in offspring by disrupting the HPG axis. These data provide critical insight into the persistent health risks posed by TBBPS.

Environmental Science & Technology↗

USGS2025

Perfluorodecanesulfonate (PFDS) induces innate immune toxicity through the NF-κB pathway in early life stage zebrafish

Perfluorodecanesulfonate (PFDS), a long-chain polyfluoroalkyl substance (PFAS), is widely detected in aquatic environments and increasingly recognized for its environmental persistence and bioaccumulative potential; however, its immunotoxicity remains poorly understood in aquatic biota. In this study, early life stage zebrafish ( Danio rerio ) were exposed to environmentally relevant concentrations of PFDS and PFOS for 120 h to better characterize the adverse effects of PFDS on aquatic organisms. Additionally, the toxicological differences between PFDS and PFOS at the same exposure concentrations were compared, as PFDS is a known substitute for PFOS. PFDS bioaccumulated in zebrafish larvae at environmentally relevant concentrations, which disrupted immune function by altering the number of macrophages and neutrophils, inducing oxidative stress, and dysregulating immune markers such as interleukins and immunoglobulins. Mechanistically, PFDS activated the nuclear factor kappa B (NF-κB) signaling pathway, driving pro-inflammatory cytokine expression and immune dysfunction. Furthermore, the use of a NF-κB morpholino knockdown confirmed the role of the NF-κB pathway in mediating PFDS-induced immunotoxicity. These findings provide the first comprehensive evidence of PFDS-induced immunotoxicity being mediated through NF-κB activation, offering novel insights into the ecological risks of long-chain perfluorosulfonic acids. Notably, PFDS exhibited a stronger immunotoxic response relative to PFOS, indicating that its adverse effects may be more severe. Overall, these findings provide valuable insights for the ecological risk assessment of PFDS and the toxic potential that unregulated PFAS can have to aquatic systems.

Environment International↗

USGS2024

Perfluorohexanesulfonic acid (PFHxS) induces hepatotoxicity through the PPAR signaling pathway in larval zebrafish (Danio rerio)

In recent years, the industrial substitution of long-chain per- and polyfluoroalkyl substances (PFAS) with short-chain alternatives has become increasingly prevalent, resulting in the widespread environmental detection of perfluorohexanesulfonic acid (PFHxS), a short-chain PFAS. However, there remains limited information about the potential adverse effects of PFHxS at environmental concentrations to wildlife. Here, early life stage zebrafish ( Danio rerio ) were exposed to environmentally relevant concentrations of PFHxS to better characterize the adverse effects of PFHxS on aquatic organisms. Nontargeted, transcriptomic analysis revealed potential hepatotoxic effects in exposed larvae, including macrovesicular and microvesicular hepatic steatosis, as well as focal liver necrosis. Morphological, histological, biochemical, and targeted transcript expression profiles further confirmed significant alterations in hepatocellular lesion numbers, liver pathological structures, relative liver size, liver biochemical parameters, and liver function genes. To validate the PPAR-mediated toxicological mechanism identified as an enriched pathway through in silico bioinformatics analysis, we tested the coexposure to an antagonist and PPAR morpholino knockdown. This intervention alleviated PFHxS-induced hepatic effects, including reductions in the levels of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and total triglycerides. Our results demonstrate that environmentally relevant concentrations of PFHxS can impair liver development and function in fish, which could have potential risks to aquatic organisms.

Environmental Science & Technology↗